Dermal Changes in the Lower Leg Skin of Patients With Venous Hypertension

Abstract

Patients with chronic venous disease may develop characteristic changes in the skin of the lower limb known as lipodermatosclerosis (LDS). The affected skin becomes indurated and pigmented and often ulcerates. The degree of induration associated with LDS correlates directly with ulcer formation and leads to a subsequent delayed rate of healing. However, there is limited information regarding the cellular and molecular events that lead from venous dysfunction to LDS development. This article reviews the current knowledge of the clinical progression of chronic venous disease, summarizing the histological findings from these authors' laboratory and other studies on LDS, and offers possible mechanisms to explain the fibrotic changes associated with this condition.

Procollagen type I gene expression and cell proliferation are increased in lipodermatosclerosis

“…It is also possible that the inflammatory phase in our LDS skin samples had resolved or, in the pre‐LDS samples, was still to occur. Therefore, although profibrotic mediators from inflammatory cells cannot be ruled out as playing a role in LDS formation, it is likely that additional factors associated with venous disease, such as the persistence of fibrin, 35 release of free radicals 36 or number of dermal dendrocytes, 37 contribute to the development of these fibrotic skin changes. Notably, patients in CEAP class 2/3 displayed little evidence of LDS but showed a similar severity and duration of chronic venous disease to those of patients in CEAP class 4 with LDS.…”

New insights into therapy by mathematical analysis: Recalcitrant granulated improved more than sclerotic venous leg ulcers with amelogenin treatment

“…This temporary matrix should provide growth structures for the fibroblasts, stimulate their migration and adhesion and finally lead to healing of the wound [6,7]. This supports the hypothesis that there may be a divergent result after treatment of granulated or sclerotic ulcerations and especially that sclerotic ulcerations may benefit more from the treatment because of their reduced potential to build up granulation tissue [8,9]. Additionally, we tried to analyse whether there is a correlation between pain intensity (measured via the visual analogue scale) and response to treatment.…”

Pseudomembranous changes in the dermis: A novel observation and potential clue for evolving lipodermatosclerosis?

“…There is increasing recognition that excessive proteolytic activity mediated by matrix metalloproteinases and fibrinolytic factors of the plasminogen activation system are involved in the pathogenesis of LDS . Fibrosis is the end result as suggested by the observation that the number of cells expressing procollagen type 1 mRNA (COL1A1) is significantly higher in the dermis of patients with LDS compared with control samples . To estimate the prevalence of pseudomembranous changes in the dermis, we reviewed the histopathologic features of 16 cases of LDS from our archives.…”